Vallbracht A, Fleischer B, Busch F W
Institut für Virologie, Universität Bremen, BRD.
Intervirology. 1993;35(1-4):133-9. doi: 10.1159/000150304.
Immunopathologic mechanisms leading to liver tissue injury in hepatitis caused by hepatitis A virus (HAV) were studied in an autologous in vitro model. Data show virus-specific killing by liver-infiltrating T lymphocytes in man and support the hypothesis that hepatocellular damage as well as efficient elimination of virus-infected hepatocytes is mediated by HLA-restricted, HAV-specific CD8+ T lymphocytes. Furthermore, experimental results demonstrate that human interferon-gamma produced by HAV-specific T cells may act as a key factor in T-cell-promoted clearance of HAV-infected hepatocytes. Besides the well-known hepatotropism, the myelotropic properties of HAV have some important clinical implications. Perturbations of hematopoietic regulation, ranging from transient granulocytopenia to rare cases of bone marrow failure, are associated with HAV infection. In an attempt to elucidate the pathogenetic mechanisms, we could show a direct suppressive effect of HAV on human bone marrow progenitors and a significant progressive decline in these cells in HAV-infected long-term bone marrow cultures.
在一个自体体外模型中研究了甲型肝炎病毒（HAV）引起的肝炎中导致肝组织损伤的免疫病理机制。数据显示人类肝脏浸润性T淋巴细胞具有病毒特异性杀伤作用，并支持以下假说：肝细胞损伤以及病毒感染肝细胞的有效清除是由HLA限制的、HAV特异性CD8 + T淋巴细胞介导的。此外，实验结果表明，HAV特异性T细胞产生的人类γ干扰素可能是T细胞促进清除HAV感染肝细胞的关键因素。除了众所周知的嗜肝性外，HAV的嗜髓性具有一些重要的临床意义。从短暂性粒细胞减少到罕见的骨髓衰竭，造血调节的紊乱都与HAV感染有关。为了阐明发病机制，我们发现HAV对人类骨髓祖细胞有直接抑制作用，并且在HAV感染的长期骨髓培养中这些细胞显著逐渐减少。
